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Transcriptomic analysis of Bptf wild-type and Bptf heterozygous lymphomas arising from Em-Myc tumors

ABSTRACT: Purpose: Evaluation of the impact of a reduction in Bptf levels on the nature of lymphomas arising from Em-Myc mice. Results: Bptf heterozygous tumors show reduced activity of the E2F and c-MYC pathways, together with increased activity of the NF-kB pathway.

ORGANISM(S): Mus musculus

PROVIDER: GSE141647 | GEO | 2019/12/10

REPOSITORIES: GEO

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Transcriptomic analysis of Bptf wild-type and Bptf heterozygous lymphomas arising from Em-Myc tumors

Project description:Transcriptomic analysis of Bptf wild-type and Bptf heterozygous lymphomas arising from Em-Myc tumors

| PRJNA594301 | ENA

Expression data from Em-Myc mouse lymphomas

Project description:Ezh2 encodes for the catalyc unit of the PRC2 complex. RNAi-mediated suppressing of Ezh2 by two independent shRNAs promotes Em-myc lymphomagenesis in vivo. Microarray were used to explore the trascriptional changes driven by suppression of Ezh2 in Em-myc cells and to identify which programs contribute to promotion of lymphoma formation. RNA was extracted from purified primary lymphoma cells for each shRNAs targeting Ezh2 and from two independent preparations of premalignant Em-myc cells. Mouse Genome 1.0 ST arrays were processed according to the manifacturer`s instructions.

2015-02-01 | E-GEOD-64537 | biostudies-arrayexpress

Expression data from Em-Myc mouse lymphomas

2015-02-01 | GSE64537 | GEO

BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [RNA-Seq]

Project description:The c-MYC oncogene is a key transcription factor deregulated in most human tumors. Histone marks associated with transcriptionally active genes in euchromatic islands define the set of high-affinity c-MYC targets. The mechanisms involved in their recognition by c-MYC are not known but likely involve chromatin-remodelling and chromatin-modifying complexes. Here, we show that c-MYC interacts with BPTF, a core subunit of the NURF complex that binds active chromatin. BPTF is required for the activation of the full c-MYC transcriptional programme in fibroblasts. BPTF knockdown leads to a decrease in c-MYC recruitment to DNA and to changes in chromatin accessibility. Using BPTF-null MEFs we show that BPTF is necessary for c-MYC-driven proliferation, G1-S progression, and replication stress, but not for c-MYC-driven apoptosis. Consistently, BPTF is required for the proliferation of cells driven by c-MYC, such as Burkitt lymphoma, and its expression in human cancer lines correlates with the activation of c-MYC gene signatures. Our findings point to the c-MYC-BPTF axis as a potential therapeutic target in cancer. To assess whether BPTF is required for the transcriptional activity of c-MYC, human foreskin fibroblasts (HFF) were stably transduced with the chimeric MYC-ER cDNA (HFF MYC-ER) and infected with lentiviruses coding for either control (shNt) or BPTF-targeting shRNAs. Cells were serum-starved for 2 days to achieve quiescence and then treated with 4-hydroxytamoxifen (4-OHT)

2016-01-19 | E-GEOD-65545 | biostudies-arrayexpress

BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [ChIP-Seq]

2016-01-19 | E-GEOD-65544 | biostudies-arrayexpress

BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [ChIP-Seq]

2016-01-19 | GSE65544 | GEO

BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [RNA-Seq]

2016-01-19 | GSE65545 | GEO

Impact of CDK4-deficiency on EM-BM-5-myc driven B-lymphoma

Project description:Impact of CDK4-deficiency on EM-BM-5-myc driven B-lymphoma By crossing mating CDK4 Knockout mice with EM-BM-5-myc mice,We found CDK4-deficiency enhances the EM-BM-5-myc induced B-lymphoma.We further to discover the molecular mechanism B-lymphoma cells form the cdk4+/+ EM-BM-5-myc and cdk4-/-EM-BM-5-myc mice and then culturing for RNA extraction and hybridization on Affymetrix microarrays.

2012-12-16 | E-GEOD-21683 | biostudies-arrayexpress

BPTF Depletion Enhances NK Cell Mediated Antitumor Immunity

Project description:In mouse models, the bromodomain PHD finger transcription factor (BPTF) chromatin remodeling subunit in tumor cells suppresses natural killer (NK) cell antitumor activity. In vitro, BPTF suppresses NK cell cytolytic activity to mouse and human cancer cell lines, demonstrating a conserved function.

2017-04-28 | GSE85756 | GEO

BPTF inhibitor increases gastric cancer response to Erlotinib by epigenetically regulating c-MYC/PLCG1/pErk axis [RNA-seq]

Project description:To understand how BPTF conferred resistance to Erlotinib in GC cells, we performed transcriptome profiling (RNA-seq) in MGC803/BPTF-KO and MGC803/BPTF-NC cells.

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